Social episodic memory in severe alcohol use disorder: Positive encoding bias and negative bias in accessibility of interpersonal information.

BACKGROUND: Alterations in higher-order social cognition are well documented in individuals with severe alcohol use disorder (SAUD). However, the basic mechanisms underpinning them are not well understood. This knowledge gap hampers the development of targeted therapeutic interventions. Here, we investigated whether individuals with SAUD show abnormalities in social episodic memory processes, which may represent relevant candidate mechanisms for alterations in social cognition. METHODS: Recently detoxified patients with SAUD and matched healthy controls (HCs) completed two experimental tasks. We first used a Social Recognition Task in 40 SAUD patients and 40 HCs to measure the participants' ability to implicitly memorize the facial identity and emotion of novel interpersonal cues (i.e., dynamic facial expressions of anger and happiness). We then used a Social Memory Accessibility Task in 29 SAUD patients and 30 HCs) to measure participants' access to and fluency for already existing social memories by asking them to retrieve as many specific positive and negative interpersonal events as possible within equal time limits. RESULTS: In the Social Recognition Task, we found that, compared to HCs, patients with SAUD had a globally lower recognition performance for the facial identities of novel social stimuli, but a preserved bias toward positive information. Conversely, in the social memory accessibility task, patients showed greater access to and fluency for negative interpersonal memories than controls (no group differences were observed for positive ones), resulting in a negative accessibility bias. CONCLUSIONS: This exploration of episodic social memory in individuals with SAUD showed (1) a preserved bias for the encoding of positive versus negative novel social information, and (2) greater access to negative than positive interpersonal memories. These results enhance our understanding of socio-affective processing in individuals with SAUD and identify social memory alterations that may contribute to social cognition and interpersonal difficulties.

Role of the Microbiome and the Gut-Brain Axis in Alcohol Use Disorder: Potential Implication for Treatment Development.

The gut microbiota is constituted by trillions of microorganisms colonizing the human intestine. Studies conducted in patients with alcohol use disorder (AUD) have shown altered microbial composition related to bacteria, viruses, and fungi.This review describes the communication pathways between the gut and the brain, including the ones related to the bacterial metabolites, the inflammatory cytokines, and the vagus nerve. We described in more detail the gut-derived metabolites that have been shown to be implicated in AUD or that could potentially be involved in the development of AUD due to their immune and/or neuroactive properties, including tryptophan-derivatives, tyrosine-derivatives, short chain fatty acids.Finally, we discussed the potential beneficial effects of microbiome-based therapies for AUD such as probiotics, prebiotics, postbiotic, and phage therapy.

Relationship between transcranial magnetic stimulation markers of motor control and clinical recovery in obsessive compulsive disorder/Gilles de la Tourette syndrome: a proof of concept case study.

Background: Obsessive compulsive disorder (OCD) and Gilles de la Tourette syndrome (GTS) are neurodevelopmental disorders characterized by difficulties in controlling intrusive thoughts (obsessions) and undesired actions (tics), respectively. Both conditions have been associated with abnormal inhibition but a tangible deficit of inhibitory control abilities is controversial in GTS. Methods: Here, we examined a 25 years-old male patient with severe OCD symptoms and a mild form of GTS, where impairments in motor control were central. Transcranial magnetic stimulation (TMS) was applied over the primary motor cortex (M1) to elicit motor-evoked potentials (MEPs) during four experimental sessions, allowing us to assess the excitability of motor intracortical circuitry at rest as well as the degree of MEP suppression during action preparation, a phenomenon thought to regulate movement initiation. Results: When tested for the first time, the patient presented a decent level of MEP suppression during action preparation, but he exhibited a lack of intracortical inhibition at rest, as evidenced by reduced short-interval intracortical inhibition (SICI) and long-interval intracortical inhibition (LICI). Interestingly, the patient's symptomatology drastically improved over the course of the sessions (reduced obsessions and tics), coinciding with feedback given on his good motor control abilities. These changes were reflected in the TMS measurements, with a significant strengthening of intracortical inhibition (SICI and LICI more pronounced than previously) and a more selective tuning of MEPs during action preparation; MEPs became even more suppressed, or selectively facilitated depending on the behavioral condition in which they we probed. Conclusion: This study highlights the importance of better understanding motor inhibitory mechanisms in neurodevelopmental disorders and suggests a biofeedback approach as a potential novel treatment.